MARC R contact FREEMANSummaryAffiliation: University of Massachusetts Medical School Country: USA Publications
Research Grants
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Detail Information
Publications
Specification and morphogenesis of astrocytesMarc R Freeman
Department of Neurobiology, Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA
Science 330:774-8. 2010..A major challenge for the field is to understand how astrocytes talk to each other, and to neurons, during development to establish appropriate astrocytic and neuronal network architectures...
Sculpting the nervous system: glial control of neuronal developmentMarc R Freeman
Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA 01605 2324, USA
Curr Opin Neurobiol 16:119-25. 2006..These recent insights provide further compelling evidence that glial cells, through their diverse cellular actions, are essential contributors to the construction of a functionally mature nervous system...
Glial cell biology in Drosophila and vertebratesMarc R Freeman
Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA 01605 2324, USA
Trends Neurosci 29:82-90. 2006..The striking parallels that emerge from this comparison argue that invertebrate model organisms such as Drosophila have excellent potential to add to our understanding of fundamental aspects of glial biology...
Glia got rhythmPatrick Emery
Department of Neurobiology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
Neuron 55:337-9. 2007....
Glial (and neuronal) cells missingMarc R Freeman
Department of Neurobiology, University of Massachusetts Medical School, 719 Lazare Research Building, 364 Plantation Street, Worcester, Massachusetts 01605, USA
Neuron 48:163-5. 2005..A study by Chotard et al. in this issue of Neuron reveals that this "master regulator" of glial cell fate specification is also required (gasp!) to generate neurons...
The Drosophila cell corpse engulfment receptor Draper mediates glial clearance of severed axonsJennifer M MacDonald
Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
Neuron 50:869-81. 2006..Thus Draper appears to act as a glial receptor for severed axon-derived molecular cues that drive recruitment of glial processes to injured axons for engulfment...
Glia and muscle sculpt neuromuscular arbors by engulfing destabilized synaptic boutons and shed presynaptic debrisYuly Fuentes-Medel
Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts, USA
PLoS Biol 7:e1000184. 2009....
Draper-dependent glial phagocytic activity is mediated by Src and Syk family kinase signallingJennifer S Ziegenfuss
Department of Neurobiology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, Massachusetts 01605 2324, USA
Nature 453:935-9. 2008..Thus, Draper seems to be an ancient immunoreceptor with an extracellular domain tuned to modified self, and an intracellular domain promoting phagocytosis through an ITAM-domain-SFK-Syk-mediated signalling cascade...
Glial control of synaptogenesisMarc R Freeman
Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
Cell 120:292-3. 2005..In this issue of Cell, Barres and colleagues (Christopherson et al., 2005) demonstrate that glial-derived thrombospondins and additional soluble glial-secreted factors regulate synapse assembly and functional maturation...
Ensheathing glia function as phagocytes in the adult Drosophila brainJohnna Doherty
Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts 01605 2324, USA
J Neurosci 29:4768-81. 2009....
Activation of autophagy during cell death requires the engulfment receptor DraperChristina K McPhee
Department of Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
Nature 465:1093-6. 2010..Further, Drpr is the first factor that distinguishes autophagy that is associated with cell death from autophagy associated with cell survival...
Wld S requires Nmnat1 enzymatic activity and N16-VCP interactions to suppress Wallerian degenerationMichelle A Avery
Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA 01605, USA
J Cell Biol 184:501-13. 2009..Thus, nuclear Nmnat activity does not appear to be essential for Wld(S)-like axon protection...
Unwrapping glial biology: Gcm target genes regulating glial development, diversification, and functionMarc R Freeman
Institutes of Neuroscience and Molecular Biology, University of Oregon, Eugene, OR 97403, USA
Neuron 38:567-80. 2003..80% of these Drosophila glial genes have mammalian homologs; these are now excellent candidates for regulating human glial development, function, or disease...
Research Grants
- The Draper signaling pathway in Drosophila glial immune functionsMarc R Freeman; Fiscal Year: 2010..Characterizing genes that regulate neuronal and glial function in response to CNS trauma is essential to identify new avenues for the treatment of CNS injury and neurological disease. ..
- How does Wlds protect severed axons?MARC FREEMAN; Fiscal Year: 2009..Our work will identify many new molecules that will be targets for treatment of patients after brain injury or during neurological disease. ..
- Role of glia in sculpting synpatic fields during development and plasticityMARC R contact FREEMAN; Fiscal Year: 2010..Our work will provide fundamental knowledge regarding how neurons and glia communicate during the modification of synapses, and is expected to provide important insights into how glial dysfunction might cause disease. ..
- The Draper signaling pathway in Drosophila glial immune functionsMARC FREEMAN; Fiscal Year: 2007..Characterizing genes that regulate neuronal and glial function in response to CNS trauma is essential to identify new avenues for the treatment of CNS injury and neurological disease. ..
- How does Wlds protect severed axons?Marc R Freeman; Fiscal Year: 2010..Our work will identify many new molecules that will be targets for treatment of patients after brain injury or during neurological disease. ..
